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Organotypic Endothelial Cell Surface Molecules Mediate Organ Preference of Metastasis

  • Chapter
Endothelial Cell Dysfunctions

Abstract

Metastases are tumor colonies that develop in distant, often multiple organ sites by dissemination from a malignant primary tumor. Although the most frequent organ sites of distant metastases are the first organs encountered by blood-borne tumor cells, many cancers metastasize to sites which are unrelated to the initial organ entered by circulating tumor cells and, thus, display unique organ colonization patterns that do not fit simple, anatomical-mechanical trapping theories of tumor cell dissemination.1–7 For example, breast adenocarcinomas metastasize frequently to liver, bone, brain, and adrenals, in addition to the expected, high incidence of metastasis to the lungs, and carcinomas of the prostate metastasize most often to bone. This nonrandom pattern of metastasis was first described by Paget,8 who championed the “seed and soil” hypothesis of the metastatic spread. He postulated that gross tumor development was a consequence of the provision of a fertile environment (the soil) in which compatible tumor cells (the seeds) could proliferate.4 Numerous studies on the mechanisms of preferential metastasis have since shown that tumor cell implantation, invasion, survival, and growth at secondary organ sites depend upon a number of tumor cell and host characteristics that provide the proper cellular and stromal environment for metastasis to develop.9–16

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Authors and Affiliations

  1. Cancer Biology Laboratories, Department of Pathology, College of Veterinary Medicine, Cornell University, Ithaca, New York, 14853, USA

    Bendicht U. Pauli, Robert C. Johnson & Marwan E. El-Sabban

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  1. Institute of Cellular Biology and Pathology, Bucharest, Romania

    Nicolae Simionescu  & Maya Simionescu  & 

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Pauli, B.U., Johnson, R.C., El-Sabban, M.E. (1992). Organotypic Endothelial Cell Surface Molecules Mediate Organ Preference of Metastasis. In: Simionescu, N., Simionescu, M. (eds) Endothelial Cell Dysfunctions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0721-9_26

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  • DOI: https://doi.org/10.1007/978-1-4899-0721-9_26

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